Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivo

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Issue Date
2013-10Author
Haenchen, Steve D.
Utter, Jeff A.
Bayless, Adam M.
Dobrowsky, Rick T.
Davido, David J.
Publisher
Springer Verlag
Type
Article
Article Version
Scholarly/refereed, author accepted manuscript
Rights
© Journal of NeuroVirology, Inc. 2010
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Show full item recordAbstract
Previous studies have shown that herpes simplex virus type 1 (HSV-1) replication is inhibited by the cyclin-dependent kinase (cdk) inhibitor roscovitine. One roscovitine-sensitive cdk that functions in neurons is cdk5, which is activated in part by its binding partner, p35. Because HSV establishes latent infections in sensory neurons, we sought to determine the role p35 plays in HSV-1 replication in vivo. For these studies, wild-type (wt) and p35-/- mice were infected with HSV-1 using the mouse ocular model of HSV latency and reactivation. The current results indicate that p35 is an important determinant of viral replication in vivo.
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Citation
Haenchen, S.D., Utter, J.A., Bayless, A.M. et al. Journal of NeuroVirology (2010) 16: 405. doi:10.3109/13550284.2010.513030
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